Tribune QA
Georg, you have been the CEO of Tribune Therapeutics since 2021 and a Venture Partner at HealthCap since 2021, can you tell us about your background in the sector and how you helped start Tribune?
I’m a pharmacist by training from the University of Oslo. I was developing radio pharmaceuticals at Norway’s Algeta when the German pharmaceutical giant Bayer bought the company in 2013 for $2.9 billion. Algeta was a very important company for HealthCap, and the acquisition really created some positive downstream effects for biotech in Norway.
Before long, I started working at HealthCap as a medical associate looking for new investment opportunities. That’s how I met this scientist who was doing research on fibrosis which was intriguing. It was perfect for HealthCap as it was the combination of strong science combined with some de-risking elements as there was already clinical evidence for this pathway.
During the incubation phase we needed to negotiate a license with the University and set the course for development. HealthCap was instrumental in this process, and I was encouraged to spend more time incubating and seeding this company. After about 18 months, in 2021, Tribune was born.
As an unlisted preclinical biopharmaceutical company originated from Norway you are not very well known outside the industry and specialist investors, tell us about Tribune and the story behind your research.
The research is focused on battling fibrotic diseases. Fibrosis is a mechanism happening in many diseases and organs. These cells make a cascade of signaling proteins that ultimately replace healthy tissue with collagen and connective material, leading to organ failure.
Ole Kaasbøll is my co-founder and current CSO of Tribune. He is an MD, PhD and he spent his postdoc and doctorate researching these CCN proteins in the lab of Dr. Håvard Attramadal at the Oslo University Hospital.
They invested a lot of time producing high quality reagents as part of their research in the CCN biology. That proved to be a real differentiating factor in understanding how these proteins work, leading to the pivotal discovery that the CCN proteins need to be cleaved before they signal. This helped us develop a new mechanism of action which inhibits the profibrotic signaling from the CCN proteins.
We looked at about 35 different indications when mapping out a plan for Tribune. Kidney fibrosis is one of our focus areas.
You have demonstrated Proof of Concept of lung and kidney fibrosis in animal models, what is your clinical development plan for your lead asset TRX-44?
TRX-44 is our most advanced candidate. It interferes with activated pro-fibrotic CCN domains to block fibrotic signaling without the challenges faced by more limited approaches.
At this point, we are exploring the pan-fibrotic potential, looking at different disease stages, translational models where we look more beyond the anti-fibrotic effects. We are looking for which clinical endpoints we want to pursue in our early clinical development. So far, we haven’t locked in what the first clinical proof of concept is going to be.
How does the current clinical paradigm for IPF and kidney fibrosis look and what makes the TRX-44 asset suitable as a potential therapy for these diseases?
In IPF there are two approved therapies that are anti-fibrotic and that slow progression of fibrosis and slow the decline of lung function. Unfortunately, they don’t stop it. Tolerability is also a concern for these therapies. There are no approved anti-fibrotic therapies for kidney fibrosis. There are several approved drugs for the diseases that have kidney fibrosis, but they come at it from the cardiovascular or metabolic angle such as RAAS system inhibitors or SGLT2i. These are becoming standard of care. There are very important efficacious and safe medicines there, but none of them really target the fibrosis, so this remains an unmet need.
For both IPF and kidney fibrosis, the future is combination therapy. The new drugs coming in need to be able to go on top of existing therapies. That means they need to be very tolerable and be able to be combined with drugs that on the IPF side are not great in terms of tolerability. The TRX-44 mechanism of action is well positioned to go on top of and be complimentary to existing mechanisms out there today.
What can we expect from Tribune in the short to midterm, any specific milestones that an investor should keep an eye out for?
Right now, we are exploring how we approach early clinical development. By understanding the biology and applying translational models we make the most of the time before starting clinical development and position ourselves for success in clinical development. If I look out a bit further, I’m looking forward to seeing the pipeline crystalize as well. We have a lot of decisions to make, but it is an exciting time for the company and the work we and others are doing in the space.
Tribune was founded with funding from VCs such as HealthCap. How has HealthCap helped Tribune since founding and what do they bring to the table to help the company reach its goals?
Our interactions with HealthCap are frequent. They have been instrumental on the strategic level, prioritization, focus and making sure we are doing basic research that adds value. They are great to spar with when we are having these discussions.
As a new biotech company on the scene, it must be hard to build networks and get traction with established players. We’re grateful to be able to leverage the HealthCap network, whether it is with business development interactions with pharmas, with investors, consultants, recruitment – after 26 years, HealthCap has a lot to offer.
